Citation

Garrabou G, Inoriza JM, Moren C, Oliu G, Miro O, Marti MJ, Cardellach F. J. Environ. Sci. Health C Environ. Carcinog. Ecotoxicol. Rev. 2011; 29(1): 32-51.

Affiliation

Mitochondrial Research Laboratory, Muscle Research Unit, IDIBAPS-University of Barcelona, Internal Medicine Department-Hospital Clinic of Barcelona, Barcelona, Spain and Centro de Investigacion Biomedica en Red de Enfermedades Raras, (CIBERER Valencia Spain).

Copyright

(Copyright © 2011, Informa Healthcare)

DOI

10.1080/10590501.2011.551316

PMID

21424975

Abstract

The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains unestablished. Reported mitochondrial complex IV (mtCIV) inhibition, together with carboxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms and outcome. To "mitochondrially" evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial function (mtCIV activity) and oxidative stress (lipid peroxidation) in 60 poisoned patients and determined ACOP recovery depending on either normobaric or hyperbaric oxygen therapy along a 3-month follow-up. In the present article we positively evaluate mtCIV as a good marker of ACOP recovery, treatment effectiveness, and late neurological syndrome development, which advocates for hyperbaric oxygen therapy as the treatment of choice. However, we discourage its usefulness as a severity marker because of its excessive sensitivity. We additionally evaluate oxidative stress role and prognostic factors for neurological sequelae development.

Language: en